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PubMed2002

Incomplete excision of basal cell carcinoma: a prospective multicentre audit.

The audit of incomplete excision of basal cell carcinoma can be used as a parameter for clinical governance in plastic surgery units. However, there are no national standards, and all the previous reports from the UK have been retrospective and from regional units only. This 1 year prospective audit was undertaken simultaneously in the plastic surgery units of three different categories of hospital: a regional plastic surgery unit (University Hospital of South Manchester), a supraregional cancer hospital (Christie Hospital) and a district general hospital (Royal Bolton Hospital). A total of 757 lesions were excised from 600 patients, with 34 lesions (4.5%) being incompletely excised. The incidences of incomplete excision were similar in the regional unit (3.2%) and the district general hospital (3.1%), but higher in the supraregional cancer hospital (7.5%). The commonest site for incomplete excision was the eyebrow, followed by the postauricular area, the nose and the temple. There were no statistically significant differences in the distributions of the age and sex of the patients, the site and size of the lesions or the methods of repair between the three hospitals. However, there were significant differences in the distribution of syndromal, multiple and recurrent lesions, the grade of surgeon, and the clinical and histological subtypes. When the various confounding factors were adjusted by logistic regression, the variables most likely to have affected the incidence of incomplete excision were found to be grade of surgeon, minimal excision margin and histological subtype.

Adolescent↗

PubMed2000

Long-term follow-up of the first breast conservation trial: Guy' wide excision study.

Breast conservation therapy is now accepted as a proven approach for selected patients with operable breast cancer. Nevertheless, it is important to appreciate that the first randomized trials, which were carried out at Guy's Hospital, indicated the need for good local control and the increased mortality from breast cancer which occurred when treatment was sub-optimal. In the first trial 374 women aged > or = 50, with T1, T2, N0 and N1 tumours were randomized to either Halsted mastectomy and postoperative radiotherapy or wide excision and postoperative irradiation. Both groups were given 25-27 Gy to the gland fields and the wide excision group received additionally 35-38 Gy to the breast. Hence the wide excision group had no axillary surgery and subsequent axillary irradiation using what is now regarded as a low dose of radiotherapy. After 25 years, local relapse has occurred in 26% of the mastectomy group and 50% of the wide excision group (chi(2)= 21.6, P < 0.001). The breast cancer mortality rate at 25 years was 56% in the mastectomy group and 63% in those treated by wide excision (chi(2)= 5.33, P= 0.02). The first analysis of this trial indicated that increased risk of axillary relapse was restricted to N1 cases and so a second trial was conducted with entry only for those with clinically negative axillae (N0 series). Of 255 cases entered, 133 were randomized to mastectomy and 122 to wide excision. The same radiotherapy schedule was used as in the original Series. After 25 years local relapse occurred in 18% of the mastectomy cases and 54% of the wide excision group (chi(2)= 30.6, P < 0.001). There were significantly more distant relapse in the latter group (chi(2)= 6.32, P= 0.01), and a significant increase in breast cancer deaths (57% versus 44%, chi(2)= 4.27, P= 0.04). These two trials, conducted before the widespread introduction of systemic adjuvant therapy, both indicate the long-term effects of inadequate primary treatment. Inadvertent failure to treat the axilla effectively led not only to significantly increased axillary relapse rates but also to more deaths from metastatic disease.

Journal Article↗

PubMed1990

Excised patches of plasma membrane from vertebrate rod outer segments retain a functional phototransduction enzymatic cascade.

Ion channels in excised patches of plasma membrane are generally considered to be isolated from any intracellular regulation mechanisms. For example, in excised patches of vertebrate rod outer segment plasma membrane, the cGMP-activated cation channels have traditionally been studied in room light because the enzyme cascade linking photon absorption to channel closure was assumed to be inoperative. To investigate the possibility that, in fact, such excised patches retain a functional phototransduction enzymatic cascade, this same preparation was studied in darkness. Patches excised in the dark were found to retain the light sensitivity of their cGMP-induced conductance and the ability to synthesize cGMP. In the presence of guanosine 5'-[gamma-thio]triphosphate (GTP[gamma S]), a nonhydrolyzable GTP analog, light suppresses the cGMP-induced conductance irreversibly. Furthermore, inhibitors of phosphodiesterase activity reduce light sensitivity, whereas activated phosphodiesterase or activated transducin does not directly affect the channels. These results (i) establish that excised patches from rod outer segment retain functional phototransduction enzymes, (ii) support the classical view that channel opening is modulated by phosphodiesterase-mediated cGMP hydrolysis, and, most surprisingly, (iii) demonstrate that diffusion in excised patches is so restricted that local enzymes can induce variations in the concentration of small molecules. The indication that excised patches are not as simple as usually surmised opens the possibility of using them to study other intracellular transduction mechanisms.

1-Methyl-3-isobutylxanthine↗

PubMed1995

The general transcription-repair factor TFIIH is recruited to the excision repair complex by the XPA protein independent of the TFIIE transcription factor.

Recent studies have revealed that the general transcription factor TFIIH is also a general excision repair factor which, along with several other proteins, is required for transcription-independent excision reaction. As a general transcription factor, TFIIH is recruited to RNA polymerase II-promoter complex by another general transcription factor called TFIIE. We were interested in knowing whether TFIIE is also involved in recruiting TFIIH to the excision repair complex. We found that cell-free extract depleted of TFIIE carried out excision repair at a normal rate, leading us to conclude that TFIIE is not involved in recruiting TFIIH to the damage site and has no role in general excision repair. In contrast, the human damage recognition protein XPA specifically binds to TFIIH and apparently recruits it to the damage site. The carboxyl-terminal half of XPA is responsible for specific interaction with TFIIH. The C261S/C264S mutant of XPA bound the ERCC1-XPF complex normally, but failed to bind TFIIH and failed to complement an XP-A mutant cell-free extract indicating that the XPA-TFIIH interaction is essential to effecting the excision reaction. Interestingly, XPA also binds to the p34 subunit of TFIIE specifically and in competition with the p56 subunit of TFIIE. This latter interaction has no apparent role in general excision repair but may be relevant in the transcription-coupled repair reaction.

Amino Acid Sequence↗

PubMed1996

Reaction mechanism of human DNA repair excision nuclease.

Nucleotide excision repair consists of removal of the damaged nucleotide(s) from DNA by dual incision of the damaged strand on both sides of the lesion, followed by filling of the resulting gap and ligation. In humans, 14-16 polypeptides are required for the dual incision step. We have purified the required proteins to homogeneity and reconstituted the dual incision activity (excision nuclease) in a defined enzyme/substrate system. The system was highly efficient, removing >30% of the thymine dimers under optimal conditions. All of the six fractions that constitute the excision nuclease were required for dual incision of the thymine dimer substrate. However, when a cholesterol-substituted oligonucleotide was used as substrate, excision occurred in the absence of the XPC-HHR23B complex, reminiscent of transcription-coupled repair in the XP-C mutant cell line. Replication protein A is absolutely required for both incisions. The XPG subunit is essential to the formation of the preincision complex, but the repair complex can assemble and produce normal levels of 3'-incision in the absence of XPF-ERCC1. Kinetic experiments revealed that the 3'-incision precedes the 5'-incision. Consistent with the kinetic data, uncoupled 5'-incision was never observed in the reconstituted system. Two forms of TFIIH were used in the reconstitution reaction, one containing the CDK7-cyclin H pair and one lacking it. Both forms were equally active in excision. The excised oligomer dissociated from the gapped DNA in a nucleoprotein complex. In total, these results provide a detailed account of the reactions occurring during damage removal by human excision nuclease.

Cholesterol↗

PubMed2001

Base excision and DNA binding activities of human alkyladenine DNA glycosylase are sensitive to the base paired with a lesion.

The human alkyladenine DNA glycosylase has a broad substrate specificity, excising a structurally diverse group of damaged purines from DNA. To more clearly define the structural and mechanistic bases for substrate specificity of human alkyladenine DNA glycosylase, kinetics of excision and DNA binding activities were measured for several different damaged and undamaged purines within identical DNA sequence contexts. We found that 1,N(6)-ethenoadenine (epsilonA) and hypoxanthine (Hx) were excised relatively efficiently, whereas 7,8-dihydro-8-oxoguanine, O(6)-methylguanine, adenine, and guanine were not. Single-turnover kinetics of excision of Hx and epsilonA paired with T showed that excision of Hx was about four times faster than epsilonA, whereas binding assays showed that the binding affinity was about five times greater for epsilonA than for Hx. The opposing pyrimidine base had a significant effect on the kinetics of excision and DNA binding affinity of Hx but a small effect on those for epsilonA. Surprisingly, replacing a T with a U opposite Hx dramatically reduced the excision rate by a factor of 15 and increased the affinity by a factor of 7-8. The binding affinity of human alkyladenine DNA glycosylase to a DNA product containing an abasic site was similar to that for an Hx lesion.

Adenosine↗

PubMed2002

Mismatch repair in human nuclear extracts. Quantitative analyses of excision of nicked circular mismatched DNA substrates, constructed by a new technique employing synthetic oligonucleotides.

Mammalian mismatch repair (MMR) systems respond to broad ranges of DNA mismatches and lesions. Kinetic analyses of MMR processing in vitro have focused on base mismatches in a few sequence contexts, because of a lack of general and quantitative MMR assays and because of the difficulty of constructing a multiplicity of MMR substrates, particularly those with DNA lesions. We describe here simple and efficient construction of 11 different MMR substrates, by ligating synthetic oligomers into gapped plasmids generated using sequence-specific N.BstNBI nicking endonuclease, then using sequence-specific nicking endonuclease N.AlwI to introduce single nicks for initiation of 3' to 5' or 5' to 3' excision. To quantitatively assay MMR excision gaps in base-mispaired substrates, generated in human nuclear extracts lacking exogenous dNTPs, we used position- and strand-specific oligomer probes. Mispair-provoked excision along the shorter path from the pre-existing nick toward the mismatch, either 3' to 5' or 5' to 3', predominated over longer path excision by roughly 10:1 to 20:1. MMR excision was complete within 7 min, was highly specific (90:1) for the nicked strand, and was strongly mispair-dependent (at least 40:1). Nonspecific (mismatch-independent) 5' to 3' excision was considerably greater than nonspecific 3' to 5' excision, especially at pre-existing gaps, but was not processive. These techniques can be used to construct and analyze MMR substrates with DNA mismatches or lesions in any sequence context.

Base Pair Mismatch↗

PubMed1989

Clustered repair of excisable 4-nitroquinoline-1-oxide adducts in a larger fraction of genomic DNA of xeroderma pigmentosum complementation group C cells.

4-Nitroquinoline-1-oxide (4NQO) produced unstable and stable purine adducts to the DNA in human cells. Alkali-labile single-strand breaks (AL-SSBs) arose from 40% of the total adducts immediately after a 30 min alkali-denaturation of DNA. Near-ultraviolet (NUV) induced photochemical SSBs at each site of the remaining 60% adducts. Normal human, xeroderma pigmentosum group A (XPA) and C (XPC) cells removed rapidly all of the AL-SSBs and half of the 60% photobreakable adducts in a similar fashion. Thus, 60-70% labile 4NQO adducts in cells were suggested to be depurinated. Only 30-40% photo-breakable stable adducts of the total were excised almost completely in 24 h by nucleotide excision repair in normal cells, but remained unexcised in XPA cells. XPC cells excised approximately 50% of such excisable adducts in 6 h without further greater loss, as revealed by the kinetics of cumulative unscheduled DNA synthesis, excision-break accumulation and reduction in photochemical SSBs. Bimodal alkali-sucrose sedimentation profiles of photolysed DNA of growing and quiescent XPC cells following a 6 h repair of 4NQO damage presented the normal preferential excision repair in 50% of genomic DNA domains and no or greatly retarded repair in the remaining domains. In XPC cells, such a larger fraction of domain-limited repair of excisable 4NQO damage than a 10-20% fraction for UV damage was the molecular basis for more resistance to 4NQO than to UV. An XP47TO strain heterogeneous within XPC had the normal 4NQO resistance and nearly normal random repair of stable 4NQO adducts throughout genomic DNA.

4-Nitroquinoline-1-oxide↗

PubMed1983

Defective thymine dimer excision from xeroderma pigmentosum chromatin and its characteristic catalysis by cell-free extracts.

Specific excision of thymine dimers from isolated normal human and xeroderma pigmentosum (XP complementation groups A, C, D and G) chromatin was investigated under cell-free conditions. Crude extracts derived from unirradiated XP groups A, C and G cells were unable to excise dimers from their own nuclear sonicates, native chromatin and whole-cell sonicates prepared after exposure to 100 J/m2 of u.v. radiation at 254 nm, while normal-cell extracts were able to do so from all substrates including purified DNA. However, the extracts of XP groups A, C and G cells became capable of excising thymine dimers from chromatin preparations depleted of loosely bound nonhistone proteins with 0.35 M NaCl and from purified DNA. Extracts of XP group D cells catalyzed normal levels of excision from nuclear sonicates, native chromatin and 0.35 M NaCl-treated chromatin. These results suggest that none of the XP groups examined is deficient in a dimer-specific u.v. endonuclease. XP groups A, C and G cells are apparently defective in 'XP factors' present in the non-histone protein fraction, which are required for the excision of thymine dimers from chromatin. The XP group D factor appears to be different from the others. Extracts from XP groups A, C and G cells were able to complement each other with respect to dimer excision from chromatin. Novobiocin (200 micrograms/ml) completely inhibited dimer excision effected by extracts of normal cells or by complementing extracts of XP cells.

Cell Line↗

PubMed1999

A mutation in the flanking 5'-TA-3' dinucleotide prevents excision of an internal eliminated sequence from the Paramecium tetraurelia genome.

The germline chromosomes in Paramecium and other ciliated protozoa contain regions of DNA that are excised and eliminated during the development of a new macronuclear genome. Paramecium tetraurelia internal eliminated sequences (IESs) are invariably flanked by a 5'-TA-3' dinucleotide sequence that is part of a larger 8-bp terminal inverted-repeat consensus sequence. Both features, the absolutely conserved 5'-TA-3' and the remaining 6-bp terminal inverted repeat, are shared with the mariner/Tc1 class of transposons. In this article we describe a mutant cell line (AIM-2) defective in excision of a single IES from the coding region of the A51 surface antigen gene. Excision of the 370-bp IES6649 is prevented by a single A to G transition in the invariably conserved 5'-TA-3' dinucleotide. Failure to excise IES6649 also revealed a 29-bp IES located inside IES6649. Additional experiments with the previously isolated AIM-1 mutant, which also contains an internal IES, shows that alternate excision using the wild-type end of IES2591 with an end from the internal IES is extremely rare or nonexistent. These results indicate that IESs are discrete elements whose excision depends upon nucleotides located within the consensus sequence, but also suggest that additional information is required to match one end of an IES with its excision partner.

Animals↗

PubMed1986

Mutagenic DNA repair in Escherichia coli. XII. Ultraviolet mutagenesis in excision-proficient umuC and lexA (ind-) bacteria as revealed by delayed photoreversal.

Streptomycin-resistant mutations are induced in excision-proficient umuC122::Tn5 bacteria given delayed photoreversal after u.v. light. The mutations occur after much earlier photoreversal than is found with the similar induction of tryptophan-independent mutations in excision-deficient umuC bacteria and the process is not markedly influenced by the presence of Casamino acids. The yield of mutants is between 25 and 40% of that found immediately after u.v. irradiation of isogenic umu+ bacteria. Mutagenesis is not inhibited by the presence of chloramphenicol after u.v. and before photoreversal when the bacteria have also been pretreated with chloramphenicol. Loss of photoreversibility of streptomycin-resistant mutations in umu+ excision-proficient bacteria also occurs during a similar period after u.v. and is similarly unaffected by Casamino acids and chloramphenicol. The results are interpreted on a 2-step model of error-prone repair in which a misincorporation step is followed by a lesion bypass step which requires induced levels of umuC gene product, the latter step being unnecessary when the pyrimidine dimer is removed by photoreversal after the misincorporation has taken place. Differences from the same phenomenon in excision-deficient bacteria are accounted for by the fact that in excision-proficient bacteria the mutation process is initiated by excision repair rather than during normal chromosomal replication. It is suggested that loss of photoreversibility in excision-proficient umu+ bacteria may reflect the misincorporation step only, thus explaining the apparent non-inducible nature of loss of photoreversibility previously reported. The bypass step alone requires induced levels of umuD,C gene products as is evidenced by the u.v.-induction of mutations in lexA102(ind-) bacteria after delayed photoreversal.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗

PubMed1986

High frequency excision of Ty elements during transformation of yeast.

Yeast (Saccharomyces cerevisiae) transposons (Ty elements) are excised from up to 20% of supercoiled plasmids during transformation of yeast cells. The excision occurs by homologous recombination across the direct terminal repeats (deltas) of the Ty element, leaving behind a single delta in the transforming plasmid. Only the initial transforming plasmid is susceptible to excision, and no high frequency excision is observed in plasmids that have become established in transformed cells or in plasmids that are resident in cells undergoing transformation. High frequency excision from plasmids during yeast transformation is not specific for Ty elements and can be observed with other segments of plasmid DNA bounded by direct repeats. The frequency of Ty excision from supercoiled plasmids is greatly reduced when the host yeast cells contain the rad52 mutation, a defect in double-strand DNA repair. When linear or ligated-linear plasmid DNAs containing a Ty element are used for transformation, few or no excision plasmids are found among the transformant colonies. These results suggest that when a yeast cell is transformed with a supercoiled plasmid, the plasmid DNA is highly susceptible to homologous recombination for a short period of time.

DNA Repair↗

PubMed1987

Precise and imprecise somatic excision of the transposon Tc1 in the nematode C. elegans.

Eleven chromosomal products of somatic excision of Tc1 transposable elements have been cloned and sequenced. The cloning method did not involve genetic reversion; therefore the products analyzed should be representative. Six empty religated target sites were from excision of one Tc1 element inserted near actin genes on linkage group V; five were from a second Tc1 element inserted elsewhere on the same linkage group. All six products from the first element were identical in sequence to an empty target site from a second strain, indicating excision had been precise. Two of the products from the second element were also precise, whereas the other three contained four extra nucleotides at the point of excision, indicating an imprecise excision. The four nucleotides are the same in all cases and could represent two terminal nucleotides of the transposon plus a two-nucleotide target site duplication. The difference in the ratio of precise to imprecise excision at the two insertion sites suggests a possible chromosomal position effect on the pathway of Tc1 somatic excision.

Animals↗

PubMed1997

Rodent UV-sensitive mutant cell lines in complementation groups 6-10 have normal general excision repair activity.

Mammalian nucleotide excision repair is the primary enzymatic pathway for removing bulky lesions from DNA. The repair reaction involves three main steps: (i) dual incisions on both sides of the lesion; (ii) excision of the damaged base in an oligonucleotide 24-31 nt in length; (iii) filling in of the post-excision gap and ligation. We have developed assays that probe the individual steps of the reaction. Using these methods (assays for incision, excision and repair patch synthesis), we demonstrate that the mammalian excision nuclease system removes bulky lesions by incising mainly at the 22nd-25th phosphodiester bonds 5'and the 3rd-5th phosphodiester bonds 3'of the lesion, thus releasing oligonucleotides primarily 26-29 nt in length. The resulting excision gap is filled in by DNA polymerases delta and epsilon as revealed by the 'phosphorothioate repair patch assay'. When these assays were employed with cell-free extracts from the moderately UV-sensitive rodent mutants in complementation groups 6-10, we found that these mutants are essentially normal in all three steps of the repair reaction. This leads us to conclude that these cell lines have normal in vitro repair activities and that the defects in these mutants are most likely in genes controlling cellular functions not directly involved in general excision repair.

Animals↗

PubMed1998

Up-regulation of base excision repair correlates with enhanced protection against a DNA damaging agent in mouse cell lines.

DNA polymerase beta is required in mammalian cells for the predominant pathway of base excision repair involving single nucleotide gap filling DNA synthesis. Here we examine the relationship between oxidative stress, cellular levels of DNA polymerase beta and base excision repair capacity in vitro , using mouse monocytes and either wild-type mouse fibroblasts or those deleted of the DNA polymerase beta gene. Treatment with an oxidative stress-inducing agent such as hydrogen peroxide, 3-morpholinosydnonimine, xanthine/xanthine oxidase or lipopolysaccharide was found to increase the level of DNA polymerase beta in both monocytes and fibroblasts. Base excision repair capacity in vitro , as measured in crude cell extracts, was also increased by lipopolysaccharide treatment in both cell types. In monocytes lipopolysaccharide-mediated up-regulation of the base excision repair system correlated with increased resistance to the monofunctional DNA alkylating agent methyl methanesulfonate. By making use of a quantitative PCR assay to detect lesions in genomic DNA we show that lipopolysaccharide treatment of fibroblast cells reduces the incidence of spontaneous DNA lesions. This effect may be due to the enhanced DNA polymerase beta-dependent base excision repair capacity of the cells, because a similar decrease in DNA lesions was not observed in cells deficient in base excision repair by virtue of DNA polymerase beta gene deletion. Similarly, fibroblasts treated with lipopolysaccharide were more resistant to methyl methanesulfonate than untreated cells. This effect was not observed in cells deleted of the DNA polymerase beta gene. These results suggest that the DNA polymerase beta-dependent base excision repair pathway can be up-regulated by oxidative stress-inducing agents in mouse cell lines.

Animals↗

PubMed2002

S100-positive spindle cells in scars: a diagnostic pitfall in the re-excision of desmoplastic melanoma.

Distinguishing desmoplastic melanoma (DM) from scar tissue on routine microscopy can be difficult, especially in re-excision specimens, and S100 immunohistochemistry has been recommended as a useful adjunct. The purpose of this study is to evaluate the extent and nature of S100 positivity in scars. In this study, formalin-fixed paraffin archival tissues were evaluated with immunohistochemistry. Ten re-excision specimens of previously biopsied nonnevomelanocytic lesions were immunostained with the S100 and CD57 (Leu 7) antibodies. In 9 of the 10 cases, the scars contained S100-positive spindle cells, but there were no cases with CD57+ cells. Ten re-excised atypical nevi and 10 re-excised melanomas were also immunostained for the S100 protein, and all 20 cases contained S100-positive spindle cells within the scars. There was a trend toward quantitatively more S100-positive spindle cells in these nevomelanocytic re-excisions. To evaluate the nature of the spindle cells, scars from two of the nonnevomelanocytic re-excisions were further analyzed utilizing immunostains for glial fibrillary acidic protein, HMB-45, Melan-A, CD1a, factor XIIIa, and neuron specific enolase. In both scars, neuron specific enolase diffusely stained the fibroblast population, but the remaining immunostains were negative in the scar. The presence of S100-positive spindle cells in scars represents a potential diagnostic pitfall, particularly in the evaluation of re-excision specimens of DM.

Cell Count↗

PubMed1995

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. IV. Dysrhythmias after sinoatrial node excision.

BACKGROUND: Subsidiary atrial pacemakers assume control after sinoatrial (SA) node excision, and anesthetic-catecholamine interactions can produce severe bradycardia during isoflurane anesthesia. We hypothesized that epinephrine enhances atrial, atrioventricular junctional, and ventricular dysrhythmias after SA node excisions in dogs and that inhalation anesthetics would facilitate such dysrhythmias. METHODS: In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, at the His bundle, and along the sulcus terminalis. Site of the earliest atrial activation and incidences of nonatrial beats were determined in the conscious state, with methylatropine, with epinephrine, and during halothane, isoflurane, or enflurane anesthesia. RESULTS: After SA node excision, a stable, regular subsidiary atrial pacemaker rhythm resulted. Epinephrine and halothane shifted the site of earliest activation to more remote atrial sites. Epinephrine-induced ventricular escape was increased by all anesthetics tested, but atropine prevented ventricular escape. Epinephrine-induced His bundle (atrioventricular junctional) and premature ventricular beats were increased by halothane and enflurane. After SA node excision, ventricular escape occurred as a result of epinephrine-anesthetic interactions, especially during anesthesia with isoflurane. CONCLUSIONS: In dogs with excised SA nodes, anesthetic-catecholamine interaction facilitates ventricular escape, His bundle dysrhythmias, and premature ventricular beats. In addition, halothane and enflurane, more than isoflurane, facilitate ectopic ventricular tachydysrhythmias with epinephrine. Compared to intact dogs, dogs with excised SA nodes may be more susceptible to epinephrine anesthetic dysrhythmias. If findings can be extrapolated to humans, intrinsic SA node dysfunction may facilitate severe cardiac dysrhythmias with inhalation anesthetics and catecholamines.

Anesthetics↗

PubMed2001

Clinical and pathological findings in reexcision of incompletely excised basal cell carcinomas.

In common practice, patients with incompletely excised basal cell carcinomas (BCCs) are referred to elective reexcision. In previous reports, it was observed that tumor cells are found in only 50% of the reexcised specimens. The authors performed a retrospective analysis of a large series of patients to evaluate clinical and pathological findings in patients who underwent reexcision of incompletely excised BCCs. A total of 1,478 BCCs arising in 1,278 patients were excised by plastic surgeons in a plastic and reconstructive surgery department during a 4-year period. In 159 patients (10.8%), the excision was incomplete according to the pathological report. These tumors were defined as an incompletely excised BCCs. One hundred of the 159 patients with incompletely excised BCCs (62.9%) were reoperated. Residual tumor cells were found in 28 of 100 patients (28%) within the pathological specimen of the reexcised tissue (defined as positive reexcision, or +veRE). There was no correlation between +veRE and the age or sex of the patient. Location of the BCCs in the cheeks, eyelids, or ears was associated with a low percent of +veRE (10.0%, 13.3%, and 22.2% respectively). Pathological factors associated with a low percent of +veRE were dermal inflammatory infiltrate in the pathological specimen (p = 0.003) and sun damage pathological changes (p = 0.03), but there was no correlation with the pathological subtype distribution of the tumors. The authors conclude that lack of tumor cells at reexcision of incompletely excised BCCs is associated with location of the tumors in the cheeks, eyelids, and ears, and with pathological findings of dermal inflammatory infiltrates or sun damage changes. The roles of inflammatory and solar changes in the destruction of residual carcinoma cells should be investigated further.

Basal Cell Carcinoma↗